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PubMed2000

Mechanisms of the thapsigargin-induced Ca(2+) entry in in situ endothelial cells of the porcine aortic valve and the endothelium-dependent relaxation in the porcine coronary artery.

The mechanisms of the thapsigargin (TG)-induced capacitative Ca(2+) entry in in situ endothelial cells and its role in the regulation of arterial tone were investigated using front-surface fluorimetry and fura-2-loaded strips of porcine aortic valve and coronary artery. In the presence of extracellular Ca(2+), TG induced an initial rapid and a subsequent sustained elevation of cytosolic Ca(2+) concentration ([Ca(2+)](i)) in valvular strips. In the absence of extracellular Ca(2+), TG induced only a transient increase in [Ca(2+)](i). The TG-induced sustained elevation of [Ca(2+)](i) in endothelial cells was inhibited completely by 1 mM Ni(2+) and partly by 10 microM econazole and 30 microM ML-9, but not by 900 ng ml(-1) pertussis toxin or 100 microM wortmannin. Therefore, cytochrome P450 and protein phosphorylation are suggested to be involved in the TG-induced Ca(2+) influx in in situ endothelial cells. TG induced an endothelium-dependent large relaxation consisting of an initial and a late sustained relaxation in coronary arterial strip precontracted with U46619 (a thromboxane A2 analogue). Indomethacin alone had no effect, while indomethacin plus N(omega)-nitro-L-arginine (L-NOARG) markedly inhibited the sustained phase and slightly inhibited the initial phase of the TG-induced relaxation. TG induced a smaller but sustained relaxation during the 40 mM K(+)-induced precontraction than that seen during the U46619-induced precontraction. This relaxation was completely abolished by the pretreatment with indomethacin plus L-NOARG. In conclusion, both nitric oxide (NO) and endothelium-derived hyperpolarizing factor were suggested to mediate the TG-induced relaxation, while NO plays a major role in the sustained relaxation. The TG-induced sustained [Ca(2+)](i) elevation in endothelial cells was thus suggested to be mainly linked to the sustained production of NO.

Animals↗
PubMed1988

Radionuclear measurement of peripheral hemodynamics in selection of vasodilators for treatment of heart failure.

In order to select the optimal vasodilator for the treatment of patients with congestive heart failure (CHF), the acute effects of three vasodilators (isosorbide dinitrate (ISDN) 5 mg, nifedipine 10 mg, and prazosin 1 mg) on peripheral capacitance and resistance vessels (CV and RV) were evaluated by a newly devised radionuclear technique (Study 1). Thirty-six patients with chronic CHF were divided into Group A (ejection fraction (EF) greater than or equal to 35%, n = 20, mean EF: 47.2 +/- 6.5%) and B (EF less than 35%, n = 16, mean EF: 24.8 +/- 7.1%). ISDN produced the strongest CV dilatation (25% in both groups). Nifedipine reduced RV tone in Groups A and B (14% and 27%, respectively), and CV tone in Group A (6%). Prazosin had the most prominent effects on both vessels in Group B. From these results, it appeared: (a) ISDN is indicated for the cases with increased CV tone, (b) nifedipine is suitable for those with increased RV tone, (c) in cases of increased tone in both vessels, nifedipine (when EF greater than or equal to 35%) or prazosin (when EF less than 35%) is optimal. To evaluate the validity of this assignment, 49 subjects with CHF were divided into Group 1 (n = 16, increased CV tone), Group 2 (n = 17, increased RV tone), and Group 3 (n = 16, increased CV and RV tone) in Study 2. In Group 1, the changes of all indexes were not significantly different between the subjects treated with optimal drug based on the assignment (subgroup P) and those with a non-optimal drug (subgroup N) after 2 wk of therapy. In Group 2, however, improvements of RV tone, EF, and exercise duration in subgroup P were greater than those in subgroup N (31 versus 10%, 21 versus 0%, 41 versus 14%, respectively). In Group 3, the results were the same as in Group 2 (34 versus 19%, 24 versus 8%, 26 versus 9%). These findings suggested that the selection of the optimal vasodilator based on peripheral hemodynamic evaluation with a newly devised radionuclear technique permits more effective treatment of chronic CHF.

Aged↗
PubMed1993

Ca(2+)-dependent K+ channels of high conductance in smooth muscle cells isolated from rat cerebral arteries.

1. Cerebrovascular smooth muscle cells (CVSMCs) were dispersed from cerebral arteries of adult rats using collagenase and trypsin. The extracellular patch clamp technique was used to study single calcium-activated potassium channels, KCa+ channels, in these cells at 21-23 degrees C. 2. Whole-cell, current clamp recordings showed that isolated CVSMCs possessed a mean resting potential of -41 +/- 7.4 mV (n = 69), an input resistance of 3.2 +/- 0.49 G omega (n = 20) and a capacitance of 24 +/- 2.3 pF (n = 7). 3. Inside-out patches displayed a calcium-dependent potassium channel, KCa+ channel, of mean conductance 207 +/- 10 pS (n = 16) and potassium permeability 3.9 x 10(-13) cm s-1 (n = 16) in symmetrical 140 mM K+ solutions. No substate conductance level was evident. 4. This channel was highly selective for K+ over Na+ or Cs+ (permeability ratio PNa/PK < 0.05; PCs/PK < 0.05, n = 5 patches in each case). Cs+ caused a voltage-dependent block of the open channel. 5. Channel openings were detected at a threshold level of free internal calcium, [Ca2+]i = 10(-8) M, and channels were open half of the time at [Ca2+]i = 2.3 x 10(-5) M (membrane potential, Vm = +40 mV, n = 5). Over the probable physiological range of [Ca2+]i, the open probability of the KCa+ channel increased with the second power of calcium concentration. 6. Open time distributions were well fitted by the sum of two exponential terms, showing the occurrence of at least two kinetically distinguishable open states. Raising [Ca2+]i increased the time constant of the slow exponential component, but had no effect on that of the fast component. 7. At [Ca2+]i < 5 x 10(-5) M, a 14 mV depolarization in membrane potential resulted in an e-fold increase in the probability of KCa+ channels adopting an open state (n = 5). The slow time constant of the open time distributions also increased on membrane depolarization. 8. Tetraethylammonium ions applied to the cytoplasmic membrane face caused a reversible, dose-dependent reduction in current flow through the KCa+ channel. This block was characterized by a dissociation constant of 0.83 +/- 0.09 mM at Vm = +40 mV and [Ca2+]i = 10(-4) M (n = 5). 9. The lower calcium sensitivity and higher sensitivity to tetraethylammonium block distinguish this from other large conductance KCa+ channels in smooth muscle cells.

Animals↗
PubMed1989

Outward potassium currents in freshly isolated smooth muscle cell of dog coronary arteries.

Outward membrane currents were characterized in single coronary smooth muscle cells of adult beagle dogs. The cells averaged 96.4 x 7.1 microns and had a resting potential of -50.7 mV, an input resistance of 307.9 M omega, a capacitance of 32.3 pF, and a calculated membrane surface area of 4,037 microns2. The cells contracted in response to external application of acetylcholine or high K+. In voltage clamp by use of the suction pipette method, outward current began to appear at -50 mV and reached 15.2 nA at 50 mV with a current density of 376.5 microA/cm2. The current was reduced by external tetraethylammonium, Ba2+, and internal Cs+, and its reversal potential had a Nernst relation to external K+ concentration. Elevation of external Ca2+ (Ca2+o) from 0 to 0.3 mM increased total K+ current by up to 300%; elevation of internal Ca2+ (Ca2+i) to 5 x 10(-7) M by internal perfusion increased total outward current to a similar extent, suggesting a large difference in Ca2+ transmembrane sensitivity. Total whole-cell K+ current consisted of two components: an initial time-independent current (Ii) followed by a time-dependent current (It). Ii and It were through separate K+ channels based on differences in a) sensitivity to Ca2+09b) modulation by an inward Ca2+ current, c) current amplitudes and activation kinetics, and d) responses to pharmacological agents. It was the largest component, measuring 4.5 nA in 0 mM Ca2+o but increasing to 11.9 nA in 0.3 mM Ca2+o with a steep 2.5 power function. It activated with a biexponential time course; in Ca2+o-free solution, its time course was relatively insensitive to voltage changes but became voltage sensitive in the presence of Ca2+o. Further, such sensitivity was abolished or enhanced by Co2+ or Bay K 8644, respectively. We concluded that there are two types of Ca2+-sensitive K+ currents, Ii and It, in coronary smooth muscle cells. Via an inward Ca2+ channel Ca2+o strongly modulates It, both in amplitude and kinetics.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2002

Comparative capacitative calcium entry mechanisms in canine pulmonary and renal arterial smooth muscle cells.

Experiments were performed to determine whether capacitative Ca(2+) entry (CCE) can be activated in canine pulmonary and renal arterial smooth muscle cells (ASMCs) and whether activation of CCE parallels the different functional structure of the sarcoplasmic reticulum (SR) in these two cell types. The cytosolic [Ca(2+)] was measured by imaging fura-2-loaded individual cells. Increases in the cytosolic [Ca(2+)] due to store depletion in pulmonary ASMCs required simultaneous depletion of both the inositol 1,4,5-trisphosphate (InsP(3))- and ryanodine (RY)-sensitive SR Ca(2+) stores. In contrast, the cytosolic [Ca(2+)] rises in renal ASMCs occurred when the SR stores were depleted through either the InsP(3) or RY pathways. The increase in the cytosolic [Ca(2+)] due to store depletion in both pulmonary and renal ASMCs was present in cells that were voltage clamped and was abolished when cells were perfused with a Ca(2+)-free bathing solution. Rapid quenching of the fura-2 signal by 100 microM Mn(2+) following SR store depletion indicated that extracellular Ca(2+) entry increased in both cell types and also verified that activation of CCE in pulmonary ASMCs required the simultaneous depletion of the InsP(3)- and RY-sensitive SR Ca(2+) stores, while CCE could be activated in renal ASMCs by the depletion of either of the InsP(3)- or RY-sensitive SR stores. Store depletion Ca(2+) entry in both pulmonary and renal ASMCs was strongly inhibited by Ni(2+) (0.1-10 mM), slightly inhibited by Cd(2+) (200-500 microM), but was not significantly affected by the voltage-gated Ca(2+) channel (VGCC) blocker nisoldipine (10 microM). The non-selective cation channel blocker Gd(3+) (100 microM) inhibited a portion of the Ca(2+) entry in 6 of 18 renal but not pulmonary ASMCs. These results provide evidence that SR Ca(2+) store depletion activates CCE in parallel with the organization of intracellular Ca(2+) stores in canine pulmonary and renal ASMCs.

Animals↗
PubMed1992

Ca2+ currents in single myocytes from human mesenteric arteries: evidence for a physiological role of L-type channels.

1. Voltage-gated Ca2+ currents (ICa) in isolated human mesenteric arterial cells were characterized in solutions containing normal (1.5 mM) Ca2+ and elevated concentrations of divalent cations using the conventional whole-cell patch clamp technique. 2. In normal Ca2+ solution, depolarization beyond -40 mV elicited a slowly decaying ICa which reached a maximum at +10 mV and appeared to reverse between +40 and +50 mV. The amplitude of this current in a group of cells correlated with cell membrane capacitance. 3. In two of thirty-three cells a small transient component of inward current was detected in the voltage range between -40 and -10 mV when cells were held at -80 mV. This current was abolished at a holding potential of -40 mV, while the current at 10 mV was not affected. These currents were referred to as T- and L-type Ca2+ respectively. 4. Elevation of the extracellular Ca2+ concentration to 20 mM shifted the voltage dependencies of Ca2+ current activation and inactivation by approximately +20 mV; a small T-current component was then observed in seven of nine cells held at -60 mV. 5. Replacement of 1.5 mM Ca2+ with 10 mM Ba2+ increased the amplitude of the current elicited at +10 mV by a factor of 3.7 and a small barium current (IBa) through T-type Ca2+ channels was also observed in most cells studied. Activation and steady-state inactivation curves for L-type current were found to be almost identical in both solutions. The steady-state inactivation for the T-type IBa was, however, more than 30 mV more negative (half-inactivation potential of -62.6 mV) of that for L-current in 1.5 mM Ca2+ and 10 mM Ba2+ solutions (-30.4 and -24.9 mV respectively). 6. A sustained inward Ca2+ channel current was recorded in the presence of normal Ca2+ and high divalent cation concentrations during 30 s depolarizations. The amplitude of this sustained current was found to be similar to the theoretical 'window current' predicted by the overlap of the activation and inactivation functions in these solutions. 7. Examination of the inactivation of the L-type current using a two-pulse protocol with a 240 ms prepulse revealed a U-shaped potential dependency for ICa, but not for IBa, suggesting the presence of a Ca(2+)-dependent component of the inactivation process. 8. These cells resemble other arterial smooth muscle cells previously studied in that they demonstrate both T- and L-components of ICa.(ABSTRACT TRUNCATED AT 400 WORDS)

Barium↗
PubMed1990

Calcium currents in isolated rabbit coronary arterial smooth muscle myocytes.

1. Calcium inward currents were recorded from relaxed enzymatically isolated smooth muscle cells from the rabbit epicardial left descending coronary artery using a single-pipette voltage-clamp technique. Outward K+ currents were blocked with CsCl-tetraethylammonium-filled pipette solutions. 2. Relaxed coronary smooth muscle cells had a maximum diameter of 8.6 +/- 0.6 microns and a cell length of 96.7 +/- 3.3 microns when bathed in 2.5 mM [Ca2+]o. The average resting membrane potential at room temperature was -32 +/- 10 mV. The mean cell capacitance was 18.5 +/- 1.7 pF and the input resistance was 3.79 +/- 0.58 G omega. 3. Depolarizing voltage-clamp steps from a holding potential of -80 mV elicited a single time- and voltage-dependent inward current which was dependent upon extracellular [Ca2+]. In 2.5 mM [Ca2+]o, the inward current was activated at a potential of -40 mV and peaked at +10 mV. This current was inhibited by 0.5 mM-CdCl2 and 1 microM-nifedipine and was enhanced with 1 microM-Bay K 8644. No detectable low-threshold, rapidly inactivating T-type calcium current was observed. 4. The apparent reversal potential of this inward current in 2.5 mM [Ca2+]o was +70 mV and shifted by 33.0 mV per tenfold increase in [Ca2+]o. This channel was also more permeable to barium and strontium ions than to calcium ions. 5. Single calcium channel recordings with 110 mM-Ba2+ as the charge carrier revealed a mean slope conductance of 20.7 +/- 0.8 pS. 6. This calcium current (ICa) exhibited a strong voltage-dependent inactivation process. However, the steady-state inactivation curve (f infinity) displayed a slight nonmonotonic, U-shaped dependence upon membrane potential. The potential at which half of the channels were inactivated was -27.9 mV with a slope factor of 6.9 mV. The steady-state activation curve (d infinity) was also well-described by a Boltzmann distribution with a half-activation potential at -4.4 mV and a slope factor of -63 mV. ICa was fully activated at approximately +20 mV. 7. The rate of inactivation was dependent upon the species of ion carrying the current. Both Sr2+ and Ba2+ decreased the rate as well as the degree of inactivation. The tau f (fitted time constant of inactivation) curve displayed a U-shaped relationship in 2.5 mM [Ca2+]o. The reactivation process was voltage dependent and could be described by a single exponential. 8. The current amplitude and the inactivation kinetics were temperature dependent.(ABSTRACT TRUNCATED AT 400 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Ca(2+)-activated and voltage-gated K+ currents in smooth muscle cells isolated from human mesenteric arteries.

1. Smooth muscle cells were enzymatically isolated from arteries dissected from mesenteric fat removed from patients undergoing routine surgery. The whole-cell patch clamp technique was used to characterize the potassium (K+) currents and passive electrical properties of these cells, using high-K(+)-containing pipette solutions with either 0.2 mM EGTA or 10 mM EGTA and 10 mM BAPTA. 2. Cell capacitance, which is proportional to membrane surface area, was normally distributed around a value of 46 pF, and independent of artery size between 0.4 and 3.6 mm. The mean membrane potential measured under current clamp was -44.1 +/- 1.9 mV (n = 52). 3. Cells dialysed with 0.2 mM EGTA in order to weakly buffer intracellular Ca2+ demonstrated a noisy outward current with an apparent threshold near -30 mV, upon which were superimposed spontaneous transient outward currents (STOCs). In the presence, but not the absence, of extracellular Ca2+, this current was potentiated if the holding potential was depolarized into the voltage range between -40 and +50 mV. This potentiation had a bell-shaped potential dependency which reflected the activation of voltage-gated Ca2+ channels in these cells. 4. The noisy current was blocked by externally applied tetraethylammonium (the dissociation constant, Kd = 0.85 mM), as were STOCs. This current was also reduced by about 40% by 8 nM charybdotoxin, and was transiently potentiated by 10 mM caffeine. The characteristics of this current therefore suggested that it was carried by large-conductance Ca(2+)-activated K+ channels. 5. Dialysis of human mesenteric arterial cells with 10 mM EGTA and 10 mM BATPA was not able to completely suppress the Ca(2+)-activated current, and reduced by approximately 50% the amplitude of the outward current recorded at positive potentials. 6. Depolarization of strongly Ca(2+)-buffered cells in the presence of 30 mM TEA to block Ca(2+)-activated K+ channels revealed a residual outward current which had both transient and sustained components. These were blocked by 4-aminopyridine (4-AP) with a similar efficiency (Kd was 1.04 and 1.16 mM at +60 mV for transient and sustained current, respectively), but the voltage ranges over which they inactivated, and their rates of recovery from inactivation, were significantly different. 7. The transient and sustained currents had different sensitivities to external Ca2+ and Cd2+ ions. Ca2+ (5 mM) significantly reduced the amplitude and shifted the voltage dependency of inactivation of the transient but not the sustained component of the outward current. Cd2+ (0.2 mM) reduced the transient current by about 30% without affecting the sustained component amplitude.(ABSTRACT TRUNCATED AT 400 WORDS)

Cadmium↗
PubMed1999

Mechanisms of Ca2+ store depletion in single endothelial cells in a Ca(2+)-free environment.

Depletion of agonist-sensitive Ca2+ stores results in activation of capacitative Ca2+ entry (CCE) in endothelial cells. The proportion of Ca2+ stores contributing to the regulation of CCE is unknown. In fura-2/am loaded single endothelial cells freshly isolated from bovine left circumflex coronary arteries, we investigated whether a resting period in a Ca(2+)-free environment results in emptying of bradykinin-sensitive Ca2+ stores (BsS) and activation of CCE. In a Ca(2+)-free environment, depletion of BsS occurred in a time-dependent manner (59% after 10 min in Ca(2+)-free solution). This effect was prevented by inhibition of the Na(+)-Ca2+ exchange but not by a blockade of ryanodine-sensitive Ca2+ release (RsCR). In contrast to BsS, mitochondrial Ca2+ content remained unchanged in the Ca(2+)-free environment. Remarkably, activity of CCE (monitored as Mn2+ influx) did not increase after depletion of BsS in the Ca(2+)-free environment. In contrast to Mn2+ influx, the effect of re-addition of Ca2+ to elevate bulk Ca2+ concentration ([Ca2+]b) decreased with the time the cells rested in Ca(2+)-free buffer. This decrease was prevented by an inhibition of RsCR. In low Na+ conditions the effect of Ca2+ on [Ca2+]b was reduced while it did not change the time the cells rested in Ca(2+)-free solution. After a 2 min period in low Na+ conditions, ryanodine-induced Ca2+ extrusion was markedly diminished. Inhibition of RsCR re-established the effect of Ca2+ on [Ca2+]b in low Na+ conditions. Collapsing subplasmalemmal Ca2+ stores with nocodazole, increased the effect of Ca2+ on [Ca2+]b. In nocodazole-treated cells, the effect of Ca2+ on [Ca2+]b was not reduced in Ca(2+)-free environment. These data indicate that activation of CCE is not associated with the agonist-sensitive Ca2+ pools that deplete rapidly in a Ca(2+)-free environment. Subplasmalemmal ryanodine-sensitive Ca2+ stores (RsS) are emptied in Ca(2+)-free/low Na+ solution and re-sequester Ca2+ which enters the cells prior an increase in [Ca2+]b occurs. Thus, in endothelial cells there are differences in the functions of various subplasmalemmal Ca2+ stores (i.e. BsS and RsS), which include either activation of CCE or regulation of subplasmalemmal Ca2+.

Animals↗
PubMed1998

Membrane capacitance changes induced by thrombin and calcium in single endothelial cells cultured from human umbilical vein.

1. Vesicular secretion from single human umbilical vein endothelial cells (HUVECs) was monitored by changes in membrane capacitance (Cm). Secretion was evoked by dialysis with strongly buffered intracellular free Ca2+ concentrations ([Ca2+]i), flash photolysis of Ca2+-loaded DM-nitrophen or caged InsP3, or by thrombin. [Ca2+]i was monitored spectrofluorimetrically with furaptra. The results show that a large, slowly rising component of vesicular secretion requires prolonged exposure to high [Ca2+]i. 2. Cm increased during intracellular perfusion with [Ca2+] buffered in the range 1.0-20 microM. Changes in Cm comprised an initial slowly rising small component of 0.1-0.5 pF followed by a faster rising larger component of up to approximately 7 pF, seen when [Ca2+]i > 2 microM and which was maximal at 10-20 microM Ca2+. 3. Thrombin evoked rapid initial elevations of [Ca2+]i to a peak of 7.1 +/- 1.5 microM (mean +/- s.e. m., n = 5) that declined within approximately 20-30 s with thrombin present either to resting levels or to a maintained elevated level of 2.0 +/- 0.7 microM (mean +/- s.e.m., range 1.0-3.6 microM, n = 3). Transient [Ca2+]i rises were associated with small, slowly rising increases in Cm of 0.1-0.2 pF, that recovered to pre-application levels over 2-3 min. Maintained elevations of [Ca2+]i caused larger, faster-rising sustained increases in Cm to 1.14 +/- 0.12 pF (mean +/- s.e.m., n = 3). Separate specific enzyme-linked immunosorbent assay (ELISA) showed that 1.0 U ml-1 thrombin produced secretion of von Willebrand factor in HUVEC cultures. 4. Short-lived [Ca2+]i elevations with a peak of 3-25 microM and a duration of approximately 20 s generated by flash photolysis of caged InsP3 or DM-nitrophen produced either no net change in Cm, or small slow increases of approximately 0.1-0.6 pF at up to 5 fF s-1 that recovered to pre-flash levels over 2-3 min. 5. Maintained elevations of [Ca2+]i in the range 1-28 microM produced by flash photolysis of DM-nitrophen caused large increases in Cm, up to approximately 4 pF, corresponding to approximately 25-30 % of the initial cell Cm. The maximum rate of change of Cm was up to 50 fF s-1 at steady [Ca2+] up to 20 microM; Cm recovered towards pre-flash levels only when [Ca2+] had declined.

Acetates↗
PubMed1992

Ionic currents in single smooth muscle cells of the canine renal artery.

Membrane currents from single smooth muscle cells enzymatically isolated from canine renal artery were recorded using the patch-clamp technique in the whole-cell and cell-attached configurations. These cells exhibited a mean resting potential, input resistance, membrane time constant, and cell capacitance of -51.8 +/- 2.1 mV, 5.2 +/- 0.98 G omega, 116.2 +/- 16.4 msec, and 29.1 +/- 2.0 pF, respectively. Inward current, when elicited from a holding potential of -80 mV, activated near -50 mV, reached a maximum near 0 mV and was sensitive to the dihydropyridine agonist Bay K 8644 and dihydropyridine antagonist nisoldipine. Two components of macroscopic outward current were identified from voltage-step and ramp depolarizations. The predominant charge carrier of the net outward current was identified as K+ by tail-current experiments (reversal potential, -61.0 +/- 0.8 mV in 10.8 mM [K+]o 0 mM [K+]i). The first component was a small, low-noise, voltage- and time-dependent current that activated between -40 and -30 mV (IK(dr)), and the second component was a larger, noisier, voltage- and time-dependent current that activated at potentials positive to +10 mV (IK(Ca)). Both IK(dr) and IK(Ca) displayed little inactivation during long (4-second) voltage steps. IK(Ca) and IK(dr) could be pharmacologically separated by using various Ca2+ and K+ channel blockers. IK(Ca) was substantially inhibited by external NiCl2 (500 microM), CdCl2 (300 microM), EGTA (5 mM), tetraethylammonium (Ki at +60 mV, 307 microM), and charybdotoxin (100 nM) but was insensitive to 4-aminopyridine (0.1-10 mM). IK(dr) was inhibited by 4-aminopyridine (Ki at +10 mV, 723 microM) and tetraethylammonium (Ki at +10 mV, 908 microM) but was insensitive to external NiCl2 (500 microM), CdCl2 (300 microM), EGTA (5 mM), and charybdotoxin (100 nM). Two types of single K+ channels were identified in cell-attached patches. The most abundant K+ channel that was recorded exhibited voltage-dependent activation, was blocked by external tetraethylammonium (250 microM), and had a large single-channel conductance (232 +/- 12 pS with 150 mM K+ in the patch pipette, 130 +/- 17 pS with 5.4 mM K+ in the patch pipette). The second channel was also voltage dependent, was blocked by 4-aminopyridine (5 mM), and exhibited a smaller single-channel conductance (104 +/- 8 pS with 150 mM K+ in the patch pipette, 57 +/- 6 pS with 5.4 mM K+ in the patch pipette). These results suggest that depolarization of canine renal artery cells opens dihydropyridine-sensitive Ca2+ channels and at least two K+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗